scholarly journals Myocardial volume and organization are changed by failure of addition of secondary heart field myocardium to the cardiac outflow tract

2003 ◽  
Vol 228 (2) ◽  
pp. 152-160 ◽  
Author(s):  
T. Mesud Yelbuz ◽  
Karen L. Waldo ◽  
Xiaowei Zhang ◽  
Marzena Zdanowicz ◽  
Jeremy Parker ◽  
...  
Keyword(s):  
Outflow Tract ◽  
Heart Field ◽  
Secondary Heart Field ◽  
Cardiac Outflow

scholarly journals Msx1 and Msx2 regulate survival of secondary heart field precursors and post-migratory proliferation of cardiac neural crest in the outflow tract

2007 ◽  
Vol 308 (2) ◽  
pp. 421-437 ◽  
Author(s):  
Yi-Hui Chen ◽  
Mamoru Ishii ◽  
Jingjing Sun ◽  
Henry M. Sucov ◽  
Robert E. Maxson
Keyword(s):  
Neural Crest ◽  
Outflow Tract ◽  
Cardiac Neural Crest ◽  
Heart Field ◽  
Secondary Heart Field

Pitx2cpatterns anterior myocardium and aortic arch vessels and is required for local cell movement into atrioventricular cushions

Development ◽  
2002 ◽  
Vol 129 (21) ◽  
pp. 5081-5091 ◽  
Author(s):  
Chengyu Liu ◽  
Wei Liu ◽  
Jennifer Palie ◽  
Mei Fang Lu ◽  
Nigel A. Brown ◽  
...  
Keyword(s):  
Aortic Arch ◽  
Pulmonary Veins ◽  
Cell Movement ◽  
Branchial Arch ◽  
Outflow Tract ◽  
Major Function ◽  
Atrioventricular Cushions ◽  
Heart Field ◽  
Left Right Asymmetry ◽  
Secondary Heart Field

Inactivation of the left-right asymmetry gene Pitx2 has been shown, in mice, to result in right isomerism with associated defects that are similar to that found in humans. We show that the Pitx2c isoform is expressed asymmetrically in a presumptive secondary heart field within the branchial arch and splanchnic mesoderm that contributes to the aortic sac and conotruncal myocardium. Pitx2c was expressed in left aortic sac mesothelium and in left splanchnic and branchial arch mesoderm near the junction of the aortic sac and branchial arch arteries. Mice with an isoform-specific deletion of Pitx2c had defects in asymmetric remodeling of the aortic arch vessels. Fatemapping studies using a Pitx2 cre recombinase knock-in allele showed that daughters ofPitx2-expressing cells populated the right and left ventricles,atrioventricular cushions and valves and pulmonary veins. In Pitx2mutant embryos, descendents of Pitx2-expressing cells failed to contribute to the atrioventricular cushions and valves and the pulmonary vein,resulting in abnormal morphogenesis of these structures. Our data provide functional evidence that the presumptive secondary heart field, derived from branchial arch and splanchnic mesoderm, patterns the forming outflow tract and reveal a role for Pitx2c in aortic arch remodeling. Moreover, our findings suggest that a major function of the Pitx2-mediated left right asymmetry pathway is to pattern the aortic arches, outflow tract and atrioventricular valves and cushions.

scholarly journals Conotruncal myocardium arises from a secondary heart field

Development ◽  
2001 ◽  
Vol 128 (16) ◽  
pp. 3179-3188 ◽  
Author(s):  
Karen L. Waldo ◽  
Donna H. Kumiski ◽  
Kathleen T. Wallis ◽  
Harriett A. Stadt ◽  
Mary. R. Hutson ◽  
...  
Keyword(s):  
Heart Development ◽  
Outflow Tract ◽  
Heart Tube ◽  
In Ovo ◽  
Atrioventricular Canal ◽  
Lateral Plate ◽  
Heart Field ◽  
Dorsal Mesocardium ◽  
Heart Fields ◽  
Secondary Heart Field

The primary heart tube is an endocardial tube, ensheathed by myocardial cells, that develops from bilateral primary heart fields located in the lateral plate mesoderm. Earlier mapping studies of the heart fields performed in whole embryo cultures indicate that all of the myocardium of the developed heart originates from the primary heart fields. In contrast, marking experiments in ovo suggest that the atrioventricular canal, atria and conotruncus are added secondarily to the straight heart tube during looping. The results we present resolve this issue by showing that the heart tube elongates during looping, concomitant with accretion of new myocardium. The atria are added progressively from the caudal primary heart fields bilaterally, while the myocardium of the conotruncus is elongated from a midline secondary heart field of splanchnic mesoderm beneath the floor of the foregut. Cells in the secondary heart field express Nkx2.5 and Gata-4, as do the cells of the primary heart fields. Induction of myocardium appears to be unnecessary at the inflow pole, while it occurs at the outflow pole of the heart. Accretion of myocardium at the junction of the inflow myocardium with dorsal mesocardium is completed at stage 12 and later (stage 18) from the secondary heart field just caudal to the outflow tract. Induction of myocardium appears to move in a caudal direction as the outflow tract translocates caudally relative to the pharyngeal arches. As the cells in the secondary heart field begin to move into the outflow or inflow myocardium,they express HNK-1 initially and then MF-20, a marker for myosin heavy chain. FGF-8 and BMP-2 are present in the ventral pharynx and secondary heart field/outflow myocardium, respectively, and appear to effect induction of the cells in a manner that mimics induction of the primary myocardium from the primary heart fields. Neither FGF-8 nor BMP-2 is present as inflow myocardium is added from the primary heart fields. The addition of a secondary myocardium to the primary heart tube provides a new framework for understanding several null mutations in mice that cause defective heart development.

scholarly journals Outflow Tract Formation—Embryonic Origins of Conotruncal Congenital Heart Disease

2021 ◽  
Vol 8 (4) ◽  
pp. 42
Author(s):  
Sonia Stefanovic ◽  
Heather C. Etchevers ◽  
Stéphane Zaffran
Keyword(s):  
Congenital Heart ◽  
Cardiac Development ◽  
Heart Defects ◽  
Dynamic Structure ◽  
Cell Types ◽  
Outflow Tract ◽  
Heart Tube ◽  
Heart Field ◽  
Multiple Cell ◽  
The Many

Anomalies in the cardiac outflow tract (OFT) are among the most frequent congenital heart defects (CHDs). During embryogenesis, the cardiac OFT is a dynamic structure at the arterial pole of the heart. Heart tube elongation occurs by addition of cells from pharyngeal, splanchnic mesoderm to both ends. These progenitor cells, termed the second heart field (SHF), were first identified twenty years ago as essential to the growth of the forming heart tube and major contributors to the OFT. Perturbation of SHF development results in common forms of CHDs, including anomalies of the great arteries. OFT development also depends on paracrine interactions between multiple cell types, including myocardial, endocardial and neural crest lineages. In this publication, dedicated to Professor Andriana Gittenberger-De Groot and her contributions to the field of cardiac development and CHDs, we review some of her pioneering studies of OFT development with particular interest in the diverse origins of the many cell types that contribute to the OFT. We also discuss the clinical implications of selected key findings for our understanding of the etiology of CHDs and particularly OFT malformations.

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